Amyloidoses are pathological conditions characterized by the aggregation of certain proteins into harmful oligomers and deposits called amyloid fibrils. These self-associated amyloid species are toxic to various types of cells, including certain type of brain cells. A particularly prominent example of an amyloidosis is Alzheimer's disease. In Alzheimer's disease, amyloid oligomers and fibrils accumulate in the brain, deteriorating the brain's memory functions.
The amyloid oligomers and fibril deposits in the brain of a patient with Alzheimer's disease are formed from a particular peptide called amyloid-beta peptide. Amyloid-beta peptide, which is also referred to “Aβ”, is a protein of about 40-43 amino acid residues. Its 40 amino acid form (Aβ 1-40), 42 amino acid form (Aβ1-42), and 43 amino acid form (Aβ1-43) have been associated with amyloid oligomer formation and fibril deposits. Amyloid-beta peptide is the major constituent of neuritic plaque deposits, which are distributed throughout the walls of cerebral blood vessels and the neuropil of the central nervous system.
Approximately five million Americans are currently afflicted with Alzheimer's disease (“AD”), with a new case identified every 70 seconds. The AD diagnosis places each patient on an irrevocable path of fatal neurodegeneration, as there is currently no effective cure for this devastating disease. At present, the treatment options for Alzheimer's disease include cholinesterase inhibitor-type and receptor agonist-type drugs. These drugs help somewhat, but are not fully effective.